Mechanism of long non‑coding RNA metastasis‑associated lung adenocarcinoma transcript 1 in lipid metabolism and inflammation in heart failure

A novel circulating biomarker lnc‐MALAT1 for acute myocardial infarction: Its relationship with disease risk, features, cytokines, and major adverse cardiovascular events

“…According to previous studies, lipid profile, cTnI, infarct size, inflammation, and adhesion molecules are viewed as hallmarks of AMI 22 , 23 , 24 ; thus, we explored the association of lnc‐MALAT1 with them among AMI patients, which showed that lnc‐MALAT1 was positively linked with lipid dysregulation (reflected by LDL‐C), the marker of myocardial injury (reflected by cTnI), disease severity indicator (reflected by infarct size), systematic inflammation (reflected by CRP, TNF‐α, IL‐6, and IL‐17A), and adhesion cytokines (reflected by VCAM‐1 and ICAM‐1). The potential explanations might be that (1) lnc‐MALAT1 could accelerate lipid metabolism and lipid oxidation in AMI, which resulted in elevated LDL‐C 25 ; (2) lnc‐MALAT1 might promote cardiomyocyte injury through several mechanisms, such as regulating autophagy‐related 3, as well as phosphatase and tensin homolog deleted on chromosome 10, which led to increased cTnI and infarct size in AMI 26 , 27 ; (3) lnc‐MALAT1 might be able to accelerate inflammation by regulating several signaling pathways, including Wnt/β‐catenin and nuclear factor‐kappa B signaling; thereby, lnc‐MALAT1 was positively associated with inflammation in AMI patients 28 , 29 ; and (4) lnc‐MALAT1 could accelerate the production of adhesion molecules through several methods, such as microRNA‐590 and the signal transducer and activator of transcription 3 pathway 21 ; thus, a positive relation was found in lnc‐MALAT1 with adhesion cytokines among AMI patients. In addition, we also discovered that higher lnc‐MALAT1 was linked with a history of DM among AMI patients.…”

Investigating microRNAs in diabetic cardiomyopathy as tools for early detection and therapeutics

“…Further, our in silico analysis revealed that its target genes were enriched in insulin signaling (p value: 0.003; fold enrichment: 5.9) and adrenergic signaling (p value: 0.02; fold enrichment: 3.7) pathways both of which becomes unresponsive during cardiac failure [57]. Zhao et al have concluded miR-532-3p to be involved in atherosclerotic plaque formation and suggested that it can be utilized for therapeutic purposes by regulating its expression [58]. Exosomal mir-672-5p has also been studied for therapeutic applications in spinal cord injury as it targets Caspase-1 signaling pathway [59].…”

The Emerging Roles of the β-Secretase BACE1 and the Long Non-coding RNA BACE1-AS in Human Diseases: A Focus on Neurodegenerative Diseases and Cancer

“… Zhuang et al (2021) showed that lncRNA OIP5-AS1 that is highly found in striated muscles endures regulation in heart development, and mice models showed more severe HF under induction by pressure overload compared to healthy controls. In another study, Zhao et al (2021) demonstrated that lncRNA MALAT1 is significantly upregulated in serum samples of 57 patients with HF and 40 HF rat models with an AUC of 0.918 in the prediction of patients with HF. Interestingly, MALAT1 inhibition ameliorated the degree of myocardial injury, improved the lipid metabolism, decreased inflammation in the rat models, and also relieved myocardial injury in the H9C2 cells.…”

“…Other types of amyloidoses with cardiac involvement include hereditary amyloidosis resulting from mutations in several genes, i.e., transthyretin and fibrinogen, and senile systemic amyloidosis ( Banypersad et al, 2012 ). The role and diagnostic potentials of lncRNAs in the landscape of HF have been evaluated in a number of studies ( Pang et al, 2016 ; Xu et al, 2020 ; Zhao et al, 2021 ). Zhuang et al (2021) showed that lncRNA OIP5-AS1 that is highly found in striated muscles endures regulation in heart development, and mice models showed more severe HF under induction by pressure overload compared to healthy controls.…”